Modulation of M-channel conductance by adenosine 5' triphosphate in bullfrog sympathetic B-neurones.

1. Adenosine 5' triphosphate (ATP) (0.5-500 microM) or muscarine (0.

Calcium-sensitive calcium influx in photoreceptor inner segments.

The effect of external calcium concentration ([Ca2+]o) on membrane potential-dependent calcium signals in isolated tiger salamander rod and cone photoreceptor inner segments was investigated with patch-clamp and calcium imaging techniques. Mild depolarizations led to increases in intracellular Ca2+ levels ([Ca2+]i) that were smaller when [Ca2+]o was elevated to 10 mM than when it was 3 mM, even though maximum Ca2+ conductance increased 30% with the increase in [Ca2+]o. When external calcium was lowered to 1 mM [Ca2+]o, maximum Ca2+ conductance was reduced, as expected, but the mild depolarization-induced increase in [Ca2+]i was larger than in 3 mM [Ca2+]o.

Low concentrations of muscarine potentiate M-current in bullfrog sympathetic B-neurones.

The concentration-dependence of the effect of muscarine on M-current (IM) and the underlying M-conductance (gM) in B-cells of bullfrog sympathetic ganglion was examined using whole-cell recording techniques. High concentrations of muscarine (> or = 200 nM) produced the classical suppression and over-recovery of steady-state IM at -30 mV. By contrast, low concentrations of muscarine (< or = 30 nM) shifted the gM activation curve to more negative potentials, increased the activation time constant (tau a) and increased steady-state IM.

Regulation of M-like K+ current, IKx, by Ca(2+)-dependent phosphorylation in rod photoreceptors.

An M-like K+ current (IKx) helps set the rod photoreceptor resting potential and accelerates the response to dim light. Recorded with ruptured-patch whole cell techniques, the amplitude of IKx diminished, and activation occurred at increasingly negative potentials as a function of time. In contrast, IKx was stable during nystatin perforated-patch recording.

Low-calcium-induced enhancement of chemical synaptic transmission from photoreceptors to horizontal cells in the vertebrate retina.

According to the classical calcium hypothesis of synaptic transmission, the release of neurotransmitter from presynaptic terminals occurs through an exocytotic process triggered by depolarization-induced presynaptic calcium influx. However, evidence has been accumulating in the last two decades indicating that, in many preparations, synaptic transmitter release can persist or even increase when calcium is omitted from the perfusing saline, leading to the notion of a "calcium-independent release" mechanism. Our study shows that the enhancement of synaptic transmission between photoreceptors and horizontal cells of the vertebrate retina induced by low-calcium media is caused by an increase of calcium influx into presynaptic terminals.